Strikng similarities exhibits between The Metabolic Syndrome1, 2 (also labeled Syndrome X or Primary Insulin Resistance Syndrome) and untreated GH deficiency in adults3. The most central findings in both these syndromes are abdominal/visceral obesity and insulin resistance1,4-6. Other features common to both conditions are high triglyceride and low high-density lipoprotein cholesterol concentrations, an increased prevalence of hypertension, elevated levels of plasma fibrinogen and plasminogen activator inhibitor-1 activity, premature atherosclerosis and increased mortality from cardiovascular diseases 1, 4,7-11.
The Metabolic Syndrome is associated with multiple endocrine abnormalities. They include increased cortisol secretion, blunted secretion of gonadotrophins and sex steroids and abnormalities in the GH/insulin-like growth factor-I (IGF-I) axis 12-14. With increased adiposity GH secretion is blunted with decreased mass of GH secreted per burst but without any major impact on GH secretory burst frequency 15. The serum IGF-I concentration is principally GH dependent and influences GH secretion though a negative feed-back system 16. The serum levels of IGF-I are inversely related to the percentage body fat 15. In addition, we have previously shown that the low serum IGF-I concentration in obesity is predominantly related to the amount of visceral adipose tissue and not to the amount of subcutaneous fat mass 13. These findings, together with other endocrine disturbances in central obesity, suggest that the low GH secretion which is observed is secondary to a central disturbance of the neuroendocrine regulation, including the GH/IGF-I axis.
The abdominal/visceral obesity and insulin resistance observed in The Metabolic Syndrome constitute the base for hypertension, dyslipoproteinemia and non-insulin dependent diabetes mellitus. 1 
Replacement therapy with recombinant human GH (rhGH) has demonstrated favorable effects on most of the features of GH deficiency in adults 17. Whether rhGH treatment can improve the metabolic abnormalities observed in abdominal/visceral obesity has never been investigated.